Skeletal muscle undergoes atrophy characterized by a reduction in fiber cross-sectional area, protein content, and strength in several chronic conditions including cancer, diabetes, chronic obstructive pulmonary disease, chronic heart failure, cystic fibrosis, AIDS, anorexia, and after high dose treatment with glucocorticoids (see, e.g., Glass, Nat Cell Biol., 5, 87-90 (2003) and Sandri, Physiology (Bethesda), 23, 160-170 (2008)). Skeletal muscle also undergoes atrophy when its level of neuromuscular activity is reduced, for example, because of denervation, unloading, or immobilization (Jackman et al., Am J Physiol Cell Physiol., 287, C834-43 (2004)) and due to “functional denervation”, e.g., in elderly patient with sarcopenia (Macaluso et al., Eur J Appl Physiol., 91, 450-472 (2004)). Furthermore, insufficient regeneration of skeletal muscle also causes the loss of skeletal muscle mass in diverse conditions, e.g., battle field or accidental injury (McKinnell et al., Curr Top Dev Biol. 71,113-130 (2005)). However, little is known about the triggers and/or the molecular events leading to loss of skeletal muscle mass, e.g., in disuse conditions, injury, anorexia, or chronic disease states. Accordingly, identification of triggers and/or the molecular events leading to loss of skeletal muscle mass are needed, e.g., to identify physiological mechanisms for treating conditions associated with loss of skeletal muscle mass. Treatments for preventing loss of skeletal muscle, for preventing loss of force production and for augmenting skeletal muscle regeneration are needed.